Salazar Fj

Hemodynamic effects of hypertonic saline in the conscious rat.

The present study examines the role of vasopressin and the sympathetic nervous system on the hemodynamic effects of an infusion of hypertonic saline (NaCl 1.5 M) in conscious rats. The cardiovascular response to hypertonic saline was similar in both untreated and hexamethonium-pretreated rats. Mean arterial pressure increased by 15 mmHg as a consequence of the elevation of total peripheral resistance, while cardiac index was decreased. The administration of an antagonist to the pressor activity of vasopressin in rats with intact reflexes, partially decreased mean arterial pressure and total peripheral resistance and increased cardiac index toward basal values. In contrast, the hemodynamic response to hypertonic saline was totally reverted when the vasopressin antagonist was injected in the hexamethonium-pretreated rats. The results of the present study indicate that the hypertensive response induced by hypertonic saline in conscious rats is due to the vasoconstrictor effects of both vasopressin and the sympathetic nervous system.

Effect of captopril on norepinephrine vascular contractility

In isolated aortic rings and in vitro perfused mesenteric arteries of Wistar rats the vasoconstrictor responses to norepinephrine (NE) were not affected by captopril (2 X 10(-4) M). However, captopril (1 mg/kg i.v.) in pithed Wistar rats attenuated significantly the increases in diastolic blood pressure induced by NE. In pithed rats the effect of captopril on NE diastolic blood pressure responses disappeared either in the presence of an angiotensin II (5 ng X kg-1 X min) infusion or when the rats were previously nephrectomized. These findings suggest that the effect of captopril on vascular responses to norepinephrine is mediated by an inhibition of the renin-angiotensin system and not by an antagonistic effect on alpha-adrenergic receptors.

ROLE OF RENIN-ANGIOTENSIN AND SYMPATHETIC NERVOUS SYSTEMS IN THE CHRONIC PHASE OF TWO-KIDNEY, ONE-CLIP HYPERTENSION IN RATS

The purpose of the present study was to examine the role of the renin-angiotensin and the sympathetic nervous systems during the chronic phase (greater than 16 weeks) of two-kidney, one-clip hypertension in conscious unrestrained rats. During this phase, the mean arterial pressure (MAP) (p less than 0.001) and plasma angiotensin II (31.9 +/- 1.5 to 125.8 +/- 19.9 pg/ml, p less than 0.005) were significantly increased as compared to normotensive group. Converting enzyme inhibition by captopril produced a significant decrease of MAP (181.2 +/- 8.2 to 140.0 +/- 5.5 mmHg, p less than 0.001). This hypotensive response was similar when aprotinin (a Kallikrein inhibitor) and captopril were infused simultaneously. Alpha 1-adrenergic receptor blockade by phenoxybenzamine (POB) significantly decreased but did not normalize MAP (179.8 +/- 12.4 to 135.8 +/- 10.4 mmHg, p less than 0.001). However, when infused after POB, captopril induced a further decrease of MAP to 86.7 +/- 9.4 mmHg (p less than 0.001). This MAP level was not different from that found in normotensive rats after infusion of the two drugs (83.2 +/- 5.3 mmHg). These results suggest that both the renin-angiotensin system and the sympathetic nervous system, by activating peripheral alpha 1-adrenergic receptors, maintain the high blood pressure during the chronic phase (greater than 16 weeks) of two-kidney, one-clip hypertension in conscious rats.